https://scholars.lib.ntu.edu.tw/handle/123456789/593022
標題: | Hepatitis C virus and hepatitis B virus co-infection | 作者: | Shih Y.-F. CHUN-JEN LIU |
關鍵字: | Co-infection; Direct-acting antivirals; Hepatitis B virus; Hepatitis C virus; Pegylated interferon; Reactivation | 公開日期: | 2020 | 出版社: | MDPI AG | 卷: | 12 | 期: | 7 | 起(迄)頁: | 741 | 來源出版物: | Viruses | 摘要: | Hepatitis C virus (HCV) and hepatitis B virus (HBV) co-infection can be encountered in either virus endemic countries. Co-infection can also be found in populations at risk of parenteral transmission. Previous studies demonstrated a high risk of liver disease progression in patients with HCV/HBV co-infection; thus, they should be treated aggressively. Previous evidence recommended therapy combining peginterferon (pegIFN) alfa and ribavirin for co-infected patients with positive HCV RNA. Recent trials further advise using direct-acting antivirals (DAAs) for the clearance of HCV in the co-infected patients. Reactivation of HBV has been observed in patients post-intervention, with higher risks and earlier onset in those having had HCV cured by DAA-versus pegIFN-based therapy. The mechanism of HBV reactivation is an interesting but unsolved puzzle. Our recent study revealed that in vitro HBV replication was suppressed by HCV co-infection; HBV suppression was attenuated when interferon signaling was blocked. In vivo, the HBV viremia, initially suppressed by the presence of HCV super-infection, rebounded following HCV clearance by DAA treatment and was accompanied by a reduced hepatic interferon response. In summary, major achievements in the treatment of HCV/HBV co-infection have been accomplished over the past 20 years. Future clinical trials should address measures to reduce or prevent HBV reactivation post HCV cure. ? 2020 by the authors. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85088051853&doi=10.3390%2fv12070741&partnerID=40&md5=98d700159d41f7ac62d5eabd92071b52 https://scholars.lib.ntu.edu.tw/handle/123456789/593022 |
ISSN: | 1999-4915 | DOI: | 10.3390/v12070741 | SDG/關鍵字: | daclatasvir; entecavir; glutathione reductase; hepatitis B surface antigen; hepatitis B(e) antigen; interferon; isoniazid; lamivudine; ledipasvir; ledipasvir plus sofosbuvir; neutralizing antibody; peginterferon; prednisolone; ribavirin; ritonavir; RNA directed RNA polymerase; sofosbuvir; virus DNA; antivirus agent; interferon; ribavirin; antibody response; antiviral therapy; clinical outcome; disease exacerbation; down regulation; drug efficacy; Hepatitis B virus; Hepatitis C virus; human; Human immunodeficiency virus; infection; liver stiffness; predictive value; Review; serology; sustained virologic response; treatment response; upregulation; virus load; virus replication; animal; chronic hepatitis B; clinical trial (topic); Hepacivirus; Hepatitis B virus; hepatitis C; mixed infection; mouse; organismal interaction; risk factor; virology; virus activation; Animals; Antiviral Agents; Clinical Trials as Topic; Coinfection; Hepacivirus; Hepatitis B virus; Hepatitis B, Chronic; Hepatitis C; Humans; Interferons; Mice; Microbial Interactions; Ribavirin; Risk Factors; Virus Activation; Virus Replication |
顯示於: | 臨床醫學研究所 |
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